RheumatologyTier 1Disease (DEADMAN)

Seronegative spondyloarthropathies - enteropathic arthritis

Description

Spondyloarthritis occurring with inflammatory bowel disease - Crohn disease or ulcerative colitis
The commonest extraintestinal manifestation of IBD

Two patterns - and they behave completely differently

	Peripheral type 1	Peripheral type 2	Axial
Joints	<5, asymmetric, large, lower limb	>=5, symmetric, small joints (MCP, PIP, wrist)	Sacroiliitis, spondylitis
Duration	Acute, <10 weeks, self-limiting	Chronic, months-years	Chronic, progressive
*Tracks bowel activity*	YES - flares with the colitis	NO - independent	NO - independent
HLA association	B27, B35, DRB1*0103	B44	B27 (~25-70%)
Erosive	Rarely	Occasionally	-

*The clinical question that decides treatment: does the arthritis follow the bowel or not?*
- Type 1 -> treat the bowel and the joints follow
- Type 2 and axial -> need their own therapy

Other musculoskeletal features

Peripheral arthritis in ~10-20% of IBD; axial disease in ~5-15% (sacroiliitis on imaging in up to 20-30%)
Crohn disease > ulcerative colitis
Higher risk of spondyloarthritis in IBD patients with:
- Other extraintestinal manifestations (uveitis, erythema nodosum, pyoderma gangrenosum)
- Complications of bowel disease (fistula, abscess, perianal disease)
- Colonic (large bowel) involvement in Crohn disease
Subclinical gut inflammation is present in up to 60% of primary ankylosing spondylitis, and ~5-10% develop overt IBD - the relationship runs both ways

Gut-joint axis: mucosal barrier failure -> bacterial translocation -> IL-23/IL-17 activation of enthesis-resident T cells
NOD2/CARD15 (Crohn), IL23R, HLA-B27
Aberrant lymphocyte homing - gut-derived T cells expressing alpha4beta7 and CCR9 traffic to synovium
*Explains why IL-23 blockade works in both bowel and joints, while IL-17 blockade works in joints but WORSENS bowel disease*

Recognising it

Inflammatory back pain in an IBD patient - onset <45, morning stiffness >30 min, better with exercise, night pain
Peripheral arthritis with a known IBD diagnosis - determine whether it tracks bowel activity
New IBD symptoms in a spondyloarthritis patient - diarrhoea, blood, weight loss, perianal disease, iron deficiency

Investigations

RF and anti-CCP negative
HLA-B27 - supports axial disease; ~25-70% of IBD-axSpA (lower than primary AS)
CRP/ESR - cannot distinguish bowel from joint inflammation; both raise it
Faecal calprotectin - useful to tell active bowel inflammation from a joint-only flare
Anaemia - iron deficiency (bowel loss) plus anaemia of chronic disease
X-ray/MRI sacroiliac joints if inflammatory back pain
- Radiographically indistinguishable from primary ankylosing spondylitis
Peripheral joint X-rays; ultrasound for enthesitis
Colonoscopy if bowel disease is not already established

Key differentials for joint pain in an IBD patient

Enteropathic arthritis (types 1, 2, axial)
*Arthralgia on corticosteroid withdrawal* - a very common mimic
Osteonecrosis (steroid)
Septic arthritis - higher risk on immunosuppression
Drug-induced: sulfasalazine/mesalazine, azathioprine hypersensitivity (fever + arthralgia in the first weeks), anti-TNF-induced lupus
Vitamin D deficiency and osteomalacia from malabsorption
Reactive arthritis after enteric infection (including in IBD patients)
Coeliac disease, Whipple disease

Axis: whether the arthritis follows the bowel. Then choose one drug that treats both compartments wherever possible.

A. Type 1 peripheral arthritis

B. Type 2 peripheral arthritis

Sulfasalazine - effective for peripheral joints AND the bowel (not for axial disease)
Methotrexate (useful for Crohn; less evidence in UC)
Anti-TNF if refractory
Intra-articular corticosteroid

C. Axial disease

Physiotherapy and structured exercise - the foundation, as in ankylosing spondylitis
*NSAIDs are the first-line drug in axSpA but are problematic here - they can flare IBD*
- Use the shortest course at the lowest dose; selective COX-2 inhibitors are better tolerated in IBD
*Conventional DMARDs (sulfasalazine, methotrexate) do NOT work for axial disease*
Escalate early to a TNF inhibitor

D. Choosing the biologic - the exam point

Agent	Joints	Bowel
TNF monoclonal antibodies (infliximab, adalimumab, golimumab, certolizumab)	Yes	Yes
*Etanercept*	Yes	*NO - ineffective in IBD, and may induce it*
IL-17 inhibitors (secukinumab, ixekizumab)	Yes	*AVOID - can precipitate or worsen IBD*
IL-12/23 (ustekinumab) and IL-23 (risankizumab)	Peripheral yes, axial poor	Yes
JAK inhibitors (tofacitinib, upadacitinib)	Yes	Yes (UC; upadacitinib also Crohn)
Vedolizumab (gut-selective alpha4beta7)	*No - may unmask or worsen joint disease*	Yes

*The single most examined fact: a TNF monoclonal treats both; etanercept and IL-17 inhibitors do not treat the bowel*
JAK inhibitors are attractive where both compartments need treating - assess CV, VTE and malignancy risk first

E. Adjunctive

Bone protection - DXA, calcium and vitamin D; high steroid exposure plus malabsorption
Correct iron, B12 (terminal ileal disease or resection), folate, vitamin D
Vaccination and TB screening before biologics
Physiotherapy, smoking cessation (smoking worsens both Crohn and axSpA)

F. Surgery

Crohn disease > ulcerative colitis
Uveitis - acute anterior in axial disease; chronic bilateral posterior uveitis is commoner in IBD than in primary AS
Erythema nodosum (tracks bowel activity), pyoderma gangrenosum (does not)
Primary sclerosing cholangitis - UC particularly
Osteoporosis and osteomalacia
Osteonecrosis (steroid)
Aphthous stomatitis, clubbing
Amyloidosis (rare, long-standing Crohn)
Venous thromboembolism during bowel flares
Iron deficiency and B12 deficiency

Type 1 peripheral arthritis: self-limiting, resolves within weeks, no joint damage - excellent prognosis
Type 2 peripheral arthritis: chronic, persists for years independent of the bowel
Axial disease: progressive, independent of bowel activity, and can lead to fusion
- Radiographic progression comparable to primary ankylosing spondylitis
Peripheral disease is generally less erosive than rheumatoid or psoriatic arthritis

Poor prognostic markers

Complications

Spinal fusion, restricted mobility, work disability
Osteoporotic and vertebral fracture - compounded by steroids and malabsorption
Uveitis and visual loss
Osteonecrosis of the femoral head
Drug-limited management - NSAIDs restricted by the bowel; IL-17 inhibitors excluded; more reliance on biologics earlier
Infection risk from combined bowel and joint immunosuppression

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